Forward-central two-particle correlations in p-Pb collisions at root s(NN)=5.02 TeV

Two-particle angular correlations between trigger particles in the forward pseudorapidity range (2.5 2GeV/c. (C) 2015 CERN for the benefit of the ALICE Collaboration. Published by Elsevier B. V.Peer reviewe

Event-shape engineering for inclusive spectra and elliptic flow in Pb-Pb collisions at root(NN)-N-S=2.76 TeV

Peer reviewe

Elliptic flow of muons from heavy-flavour hadron decays at forward rapidity in Pb-Pb collisions at root s(NN)=2.76TeV

The elliptic flow, v(2), of muons from heavy-flavour hadron decays at forward rapidity (2.5 <y <4) is measured in Pb-Pb collisions at root s(NN)= 2.76TeVwith the ALICE detector at the LHC. The scalar product, two- and four-particle Q cumulants and Lee-Yang zeros methods are used. The dependence of the v(2) of muons from heavy-flavour hadron decays on the collision centrality, in the range 0-40%, and on transverse momentum, p(T), is studied in the interval 3 <p(T)<10 GeV/c. A positive v(2) is observed with the scalar product and two-particle Q cumulants in semi-central collisions (10-20% and 20-40% centrality classes) for the p(T) interval from 3 to about 5GeV/c with a significance larger than 3 sigma, based on the combination of statistical and systematic uncertainties. The v(2) magnitude tends to decrease towards more central collisions and with increasing pT. It becomes compatible with zero in the interval 6 <p(T)<10 GeV/c. The results are compared to models describing the interaction of heavy quarks and open heavy-flavour hadrons with the high-density medium formed in high-energy heavy-ion collisions. (C) 2015 CERN for the benefit of the ALICE Collaboration. Published by Elsevier B.V.Peer reviewe

Value of CMR to differentiate cardiac angiosarcoma from cardiac lymphoma

publisher: Elsevier articletitle: Value of CMR to Differentiate Cardiac Angiosarcoma From Cardiac Lymphoma journaltitle: JACC: Cardiovascular Imaging articlelink: http://dx.doi.org/10.1016/j.jcmg.2014.08.011 content_type: simple-article copyright: Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.status: publishe

Quantitative and qualitative assessment of acute myocardial injury by CMR at multiple time points after acute myocardial infarction

BACKGROUND: Recent experimental studies have shown a dynamic time course of myocardial edema with an initial wave of edematous reaction within hours after reperfusion which almost resolved at 24 h. However, this dynamic pattern appears to be absent in clinical cohort studies. Thus far, no studies have combined a quantitative and qualitative assessment of acute myocardial injury in a large clinical cohort to explain these divergent findings. METHODS: A cohort of 225 patients (59 ± 11 years, 83% men) with successfully reperfused STEMI within 12 h of symptom onset were included. Quantitative measurements of myocardial damage such as T1 mapping and T2 triple short-tau inversion recovery (STIR), contrast-to-noise ratio (CNR) and their impact on area-at-risk (AAR), infarct size (IS), and myocardial salvage index (MSI) were assessed at different time points. One-way analysis of variance (ANOVA) and linear regression analysis was used to compare myocardial damage at the different time points. RESULTS: A small fraction of patients underwent CMR within 24 h of reperfusion (17/225, 7.6%). No significant variations in AAR, IS, MSI, T2 STIR CNR, or native T1 maps were observed between the different time points after reperfusion. Time of CMR was not a significant predictor of AAR (P = 0.90), IS (P = 0.27), MSI (P = 0.23) or T2 STIR CNR (P = 0.23). CONCLUSIONS: The majority of CMR exams in STEMI patients are performed outside the dynamic time window of early post-MI edema. The stable pattern of markers of acute myocardial damage at different time points suggests these markers are reliable for the prognostication of patients after STEMI.status: publishe

Impact of pericardial injury on inflammatory biomarkers early post myocardial infarction. A cardiovascular magnetic resonance (CMR) study

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Can Body Surface Microvolt T-Wave Alternans Distinguish Concordant and Discordant Intracardiac Alternans?

INTRODUCTION: There is convincing experimental evidence that cellular action potential duration (APD) alternans is arrhythmogenic but its relationship with body surface microvolt T-wave alternans (MTWA) remains unclear. We investigated the relationship between MTWA and APD alternans induced by alternating cycle length (CL) pacing in a pig model. METHODS: In 10 pigs, catheters in the right atrium (RA) and right (RV) and left ventricle (LV) allowed pacing and recording of monophasic action potentials (MAP). During RA pacing at stable 500-ms CL, LV was paced at alternating CL (505 ms and 495 ms). Changing the alternating LV (A-LV) pacing delay changes the size of the region with alternating ventricular activation. Spectral analysis of intracardiac MAP was correlated with body surface MTWA. In a similar setup (during alternating pacing in RV and LV), we investigated concordant versus discordant APD alternans. RESULTS: Pacing the LV with subtle alternating cycle lengths at short A-LV delay leads to broad QRS (97 ± 10 ms), body surface MTWA (mean Valt 4.2 ± 1.8 µV), and positive RR-interval alternans. At longer A-LV delay, not resulting in QRS widening (68 ± 5 ms), body surface RR alternans was absent but MTWA remained detectable and was even more pronounced (8.7 ± 5.1 µV, P < 0.01). During both concordant and discordant pacing MTWA was present. The precordial leads were better for detecting discordant APD alternans (8.0 ± 2.9 µV and 12.8 ± 4.52 µV, P = 0.02). CONCLUSION: MTWA is a potent technique to detect subtle and isolated intracardiac APD alternans that is artificially induced by alternating pacing. In the same model, discordant activation alternans can only be discriminated from concordant when using a quantifying approach of MTWA analysis.status: publishe

Effect of Infarct Severity on Regional and Global Left Ventricular Remodeling in Patients with Successfully Reperfused ST Segment Elevation Myocardial Infarction

PURPOSE: To evaluate the relationship between myocardial infarction ( MI myocardial infarction ) severity at magnetic resonance (MR) imaging and regional and global postinfarction left ventricular ( LV left ventricular ) remodeling. MATERIALS AND METHODS: This HIPAA-compliant study was institutional review board approved. In 186 patients, reperfused ST segment elevation MI myocardial infarction (mean age ± standard deviation, 59 years ± 11) was prospectively studied the first week and 4 months after infarction. Microvascular obstruction ( MVO microvascular obstruction ) and intramyocardial hemorrhage ( IMH intramyocardial hemorrhage ) helped define three infarct severity groups: S0, no MVO microvascular obstruction or IMH intramyocardial hemorrhage (n = 68); S1, MVO microvascular obstruction , no IMH intramyocardial hemorrhage (n = 84); and S2, MVO microvascular obstruction and IMH intramyocardial hemorrhage (n = 34). RESULTS: were compared in 40 control patients (mean age, 58 years ± 10). One-way analysis of variance or Kruskal-Wallis test with post hoc Bonferroni correction was used. Follow-up analysis was performed with paired Student t test or Mann-Whitney U test. Results Infarct severity was positively related (P < .001) to peak of troponin I, inflammatory biomarkers, area at risk, and infarct volume and inversely related to myocardial salvage ratio, systolic wall thickening ( SWT systolic wall thickening ) in the infarct, and adjacent myocardium and LV left ventricular ejection fraction ( EF ejection fraction ). At follow-up, LV left ventricular EF ejection fraction significantly improved in S0 and S1 (S0: 53% ± 8 to 56% ± 8, P < .001; S1: 48% ± 8 to 52% ± 10, P = .006), while S2 adversely remodeled with increase in LV left ventricular end-diastolic (175 mL ± 35 to 201 mL ± 40) and end-systolic (100 mL ± 24 to 115 mL ± 29) volumes (P < .001). SWT systolic wall thickening recovery in the infarct (S0: 32% ± 21 to 42% ± 24, P < .001; S1: 19% ± 13 to 29% ± 19, P < .001; S2: 11% ± 9 to 15% ± 15, P = .22) and adjacent (S0: 41% ± 19 to 52% ± 21, P < .001; S1: 32% ± 11 to 38% ± 16, P = .002; S2: 24% ± 13 to 29% ± 14, P = .092) and remote (S0: 54% ± 18 to 62% ± 20, P = .002; S1: 53% ± 18 to 57% ± 20, P = .092; S2: 50% ± 35 to 53% ± 22, P = .75) myocardium was related to infarct severity. LV left ventricular wall thinning with LV left ventricular mass decrease occurred at follow-up (S0: 110 g ± 27 to 100 g ± 27, P < .001; S1: 115 g ± 24 to 109 g ± 26, P = .019; S2: 134 g ± 35 to 117 g ± 27, P = .043). CONCLUSION: MVO microvascular obstruction and IMH intramyocardial hemorrhage significantly affect postinfarct myocardial and LV left ventricular remodeling; hemorrhagic infarcts behave worse than nonhemorrhagic infarcts, with lack of functional recovery and adverse LV left ventricular remodeling extending to remote myocardium.status: publishe